Acquired and intrinsic resistance to Vinca alkaloids appear to be a consequence of decreased drug retention. This may be due, in part, to decreased binding affinity of this class of agent to the intracellular target protein, tubulin. Pharmacokinetic data indicate that either increasing the dose of vincristine (VCR), or the frequency of administration would increase tumor response, but at the cost of enhanced toxicity. We wish to examine the use of a monoclonal antibody (McAb 5.1 Hll) to target Vinca alkaloids to rhabdomyosarcoma (RMS), and increase selectivity of therapy. The epitope recognized by this McAb is expressed on the membrane of myoblasts and myofibers during early gestation but not on adult tissues. All RMS examined express this antigen. We propose to characterize this antigen with respect to tissue distribution, molecular characteristics and turnover. The hypothesis that this surface antigen may be suitable for targeting McAb 5.1 Hll for use in imaging and delivery of McAb-Vinca conjugates will be tested. For these studies RMS lines in culture and their respective xenografts in immune-deprived mice will be used.